Gonadotropin-releasing hormone signaling pathways in an experimental ovarian tumor
Previous results showed that GnRH signaling is altered in cells from rat luteinized ovarian tumors (tumor group) because it did not activate the phospholipase C pathway, in contrast to control ovarian cells from superovulated prepubertal rats (SPO). In the present work, alternate GnRH-induced second...
Guardado en:
| Publicado: |
2003
|
|---|---|
| Materias: | |
| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00137227_v144_n7_p2957_ChamsonReig http://hdl.handle.net/20.500.12110/paper_00137227_v144_n7_p2957_ChamsonReig |
| Aporte de: |
| id |
paper:paper_00137227_v144_n7_p2957_ChamsonReig |
|---|---|
| record_format |
dspace |
| spelling |
paper:paper_00137227_v144_n7_p2957_ChamsonReig2023-06-08T14:36:11Z Gonadotropin-releasing hormone signaling pathways in an experimental ovarian tumor 2 [1 (3 dimethylaminopropyl) 3 indolyl] 3 (3 indolyl)maleimide 9 (tetrahydro 2 furyl)adenine arachidonic acid buserelin cyclic AMP gonadorelin gonadorelin agonist guanine nucleotide binding protein mitogen activated protein kinase mitogen activated protein kinase 1 phospholipase A2 phospholipase C phospholipase D progesterone animal cell animal experiment animal model article cell type controlled study enzyme activation female nonhuman ovary tumor prepuberty priority journal protein phosphorylation rat superovulation Adenylate Cyclase Animals Antineoplastic Agents, Hormonal Buserelin Carcinogens Cyclic AMP Enzyme Activation Female Gonadotropin-Releasing Hormone GTP-Binding Protein alpha Subunits GTP-Binding Protein alpha Subunits, Gi-Go Heterotrimeric GTP-Binding Proteins Luteoma Mitogen-Activated Protein Kinase 1 Mitogen-Activated Protein Kinase 3 Mitogen-Activated Protein Kinases Ovarian Neoplasms Pertussis Toxin Phospholipase D Phospholipases A Phosphorylation Progesterone Protein Kinase C Rats Rats, Sprague-Dawley Signal Transduction Tetradecanoylphorbol Acetate Tumor Cells, Cultured Previous results showed that GnRH signaling is altered in cells from rat luteinized ovarian tumors (tumor group) because it did not activate the phospholipase C pathway, in contrast to control ovarian cells from superovulated prepubertal rats (SPO). In the present work, alternate GnRH-induced second messengers such as phospholipase A2 and phospholipase D activation, cAMP production, ERK1/2 phosphorylation, and the presence of G proteins were evaluated to determine GnRH mechanism of action in tumor cells. G proteins examined were present in both cell types. Buserelin, a GnRH agonist, (1, 10, and 100 ng/ml) increased phosphatidylethanol in SPO, indicating phospholipase D activation. Only 100 ng/ml buserelin induced a significant response in the tumor group. Buserelin (100 ng/ml) increased 3H-arachidonic acid in culture media in SPO, indicating phospholipase A2 activation; no effect was observed in the tumor group. Buserelin (100 and 1000 ng/ml) induced pertussis toxin-insensitive cAMP increases in both cell types, with similar potencies. In the tumor group, buserelin (100 ng/ml) inhibited human chorionic gonadotropin-induced cAMP and progesterone; this effect was protein kinase C (PKC) dependent (inhibited by GF109203X, a PKC inhibitor). Buserelin (100 and 1000 ng/ml) induced ERK1/2 phosphorylation in both cell kinds. Buserelin-induced ERK1/2 activation was Gi/0 independent and PKC dependent. Only in the tumor group, buserelin-induced ERK1/2 activation was cAMP dependent (abolished by SQ 22536, the adenylyl cyclase inhibitor). Furthermore, dibutyryl cAMP-induced ERK1/2 activation in the tumor group was PKC dependent (inhibited by GF109203X). In conclusion, activation of phospholipases in tumor cells does not seem to mediate GnRH effects. GnRH signaling seems to involve adenylyl cyclase activation, PKC stimulation, and ERK1/2 phosphorylation. 2003 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00137227_v144_n7_p2957_ChamsonReig http://hdl.handle.net/20.500.12110/paper_00137227_v144_n7_p2957_ChamsonReig |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
2 [1 (3 dimethylaminopropyl) 3 indolyl] 3 (3 indolyl)maleimide 9 (tetrahydro 2 furyl)adenine arachidonic acid buserelin cyclic AMP gonadorelin gonadorelin agonist guanine nucleotide binding protein mitogen activated protein kinase mitogen activated protein kinase 1 phospholipase A2 phospholipase C phospholipase D progesterone animal cell animal experiment animal model article cell type controlled study enzyme activation female nonhuman ovary tumor prepuberty priority journal protein phosphorylation rat superovulation Adenylate Cyclase Animals Antineoplastic Agents, Hormonal Buserelin Carcinogens Cyclic AMP Enzyme Activation Female Gonadotropin-Releasing Hormone GTP-Binding Protein alpha Subunits GTP-Binding Protein alpha Subunits, Gi-Go Heterotrimeric GTP-Binding Proteins Luteoma Mitogen-Activated Protein Kinase 1 Mitogen-Activated Protein Kinase 3 Mitogen-Activated Protein Kinases Ovarian Neoplasms Pertussis Toxin Phospholipase D Phospholipases A Phosphorylation Progesterone Protein Kinase C Rats Rats, Sprague-Dawley Signal Transduction Tetradecanoylphorbol Acetate Tumor Cells, Cultured |
| spellingShingle |
2 [1 (3 dimethylaminopropyl) 3 indolyl] 3 (3 indolyl)maleimide 9 (tetrahydro 2 furyl)adenine arachidonic acid buserelin cyclic AMP gonadorelin gonadorelin agonist guanine nucleotide binding protein mitogen activated protein kinase mitogen activated protein kinase 1 phospholipase A2 phospholipase C phospholipase D progesterone animal cell animal experiment animal model article cell type controlled study enzyme activation female nonhuman ovary tumor prepuberty priority journal protein phosphorylation rat superovulation Adenylate Cyclase Animals Antineoplastic Agents, Hormonal Buserelin Carcinogens Cyclic AMP Enzyme Activation Female Gonadotropin-Releasing Hormone GTP-Binding Protein alpha Subunits GTP-Binding Protein alpha Subunits, Gi-Go Heterotrimeric GTP-Binding Proteins Luteoma Mitogen-Activated Protein Kinase 1 Mitogen-Activated Protein Kinase 3 Mitogen-Activated Protein Kinases Ovarian Neoplasms Pertussis Toxin Phospholipase D Phospholipases A Phosphorylation Progesterone Protein Kinase C Rats Rats, Sprague-Dawley Signal Transduction Tetradecanoylphorbol Acetate Tumor Cells, Cultured Gonadotropin-releasing hormone signaling pathways in an experimental ovarian tumor |
| topic_facet |
2 [1 (3 dimethylaminopropyl) 3 indolyl] 3 (3 indolyl)maleimide 9 (tetrahydro 2 furyl)adenine arachidonic acid buserelin cyclic AMP gonadorelin gonadorelin agonist guanine nucleotide binding protein mitogen activated protein kinase mitogen activated protein kinase 1 phospholipase A2 phospholipase C phospholipase D progesterone animal cell animal experiment animal model article cell type controlled study enzyme activation female nonhuman ovary tumor prepuberty priority journal protein phosphorylation rat superovulation Adenylate Cyclase Animals Antineoplastic Agents, Hormonal Buserelin Carcinogens Cyclic AMP Enzyme Activation Female Gonadotropin-Releasing Hormone GTP-Binding Protein alpha Subunits GTP-Binding Protein alpha Subunits, Gi-Go Heterotrimeric GTP-Binding Proteins Luteoma Mitogen-Activated Protein Kinase 1 Mitogen-Activated Protein Kinase 3 Mitogen-Activated Protein Kinases Ovarian Neoplasms Pertussis Toxin Phospholipase D Phospholipases A Phosphorylation Progesterone Protein Kinase C Rats Rats, Sprague-Dawley Signal Transduction Tetradecanoylphorbol Acetate Tumor Cells, Cultured |
| description |
Previous results showed that GnRH signaling is altered in cells from rat luteinized ovarian tumors (tumor group) because it did not activate the phospholipase C pathway, in contrast to control ovarian cells from superovulated prepubertal rats (SPO). In the present work, alternate GnRH-induced second messengers such as phospholipase A2 and phospholipase D activation, cAMP production, ERK1/2 phosphorylation, and the presence of G proteins were evaluated to determine GnRH mechanism of action in tumor cells. G proteins examined were present in both cell types. Buserelin, a GnRH agonist, (1, 10, and 100 ng/ml) increased phosphatidylethanol in SPO, indicating phospholipase D activation. Only 100 ng/ml buserelin induced a significant response in the tumor group. Buserelin (100 ng/ml) increased 3H-arachidonic acid in culture media in SPO, indicating phospholipase A2 activation; no effect was observed in the tumor group. Buserelin (100 and 1000 ng/ml) induced pertussis toxin-insensitive cAMP increases in both cell types, with similar potencies. In the tumor group, buserelin (100 ng/ml) inhibited human chorionic gonadotropin-induced cAMP and progesterone; this effect was protein kinase C (PKC) dependent (inhibited by GF109203X, a PKC inhibitor). Buserelin (100 and 1000 ng/ml) induced ERK1/2 phosphorylation in both cell kinds. Buserelin-induced ERK1/2 activation was Gi/0 independent and PKC dependent. Only in the tumor group, buserelin-induced ERK1/2 activation was cAMP dependent (abolished by SQ 22536, the adenylyl cyclase inhibitor). Furthermore, dibutyryl cAMP-induced ERK1/2 activation in the tumor group was PKC dependent (inhibited by GF109203X). In conclusion, activation of phospholipases in tumor cells does not seem to mediate GnRH effects. GnRH signaling seems to involve adenylyl cyclase activation, PKC stimulation, and ERK1/2 phosphorylation. |
| title |
Gonadotropin-releasing hormone signaling pathways in an experimental ovarian tumor |
| title_short |
Gonadotropin-releasing hormone signaling pathways in an experimental ovarian tumor |
| title_full |
Gonadotropin-releasing hormone signaling pathways in an experimental ovarian tumor |
| title_fullStr |
Gonadotropin-releasing hormone signaling pathways in an experimental ovarian tumor |
| title_full_unstemmed |
Gonadotropin-releasing hormone signaling pathways in an experimental ovarian tumor |
| title_sort |
gonadotropin-releasing hormone signaling pathways in an experimental ovarian tumor |
| publishDate |
2003 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00137227_v144_n7_p2957_ChamsonReig http://hdl.handle.net/20.500.12110/paper_00137227_v144_n7_p2957_ChamsonReig |
| _version_ |
1768544485169430528 |